title: Redox-mediated and ionizing-radiation-induced inflammatory mediators in prostate cancer development and treatment.
abstract: CONCLUSIONS
  Radiation therapy is widely used for treatment of prostate cancer. Radiation can directly damage biologically important molecules; however, most effects of radiation-mediated cell killing are derived from the generated free radicals that alter cellular redox status. Multiple proinflammatory mediators can also influence redox status in irradiated cells and the surrounding microenvironment, thereby affecting prostate cancer progression and radiotherapy efficiency.
  
  
  BACKGROUND
  Ionizing radiation (IR)-generated oxidative stress can regulate and be regulated by the production of proinflammatory mediators. Depending on the type and stage of the prostate cancer cells, these proinflammatory mediators may lead to different biological consequences ranging from cell death to development of radioresistance.
  
  
  RESULTS
  Tumors are heterogeneous and dynamic communication occurs between stromal and prostate cancer cells, and complicated redox-regulated mechanisms exist in the tumor microenvironment. Thus, antioxidant and anti-inflammatory strategies should be carefully evaluated for each patient at different stages of the disease to maximize therapeutic benefits while minimizing unintended side effects.
  
  
  CONCLUSIONS
  Compared with normal cells, tumor cells are usually under higher oxidative stress and secrete more proinflammatory mediators. Thus, redox status is often less adaptive in tumor cells than in their normal counterparts. This difference can be exploited in a search for new cancer therapeutics and treatment regimes that selectively activate cell death pathways in tumor cells with minimal unintended consequences in terms of chemo- and radio-resistance in tumor cells and toxicity in normal tissues.
authors.affiliation: 1 Graduate Center for Toxicology, University of Kentucky , Lexington, Kentucky.
authors.forename: Lu
authors.initials: L
authors.lastname: Miao
authors.forename: Aaron K
authors.initials: AK
authors.lastname: Holley
authors.forename: Yanming
authors.initials: Y
authors.lastname: Zhao
authors.forename: William H
authors.initials: WH
authors.lastname: St Clair
authors.forename: Daret K
authors.initials: DK
authors.lastname: St Clair
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D010084:Oxidation-Reduction; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000532:radiotherapy*; D011839:Radiation, Ionizing; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species